Gd-DTPA Enhancement of the Cisternal Portion of the Oculomotor Nerve on MR Imaging

Alexander S. Mark, 1'9 Pamela Blake,2

·7 Scott W ." Atlas,3 Michael Ross,4 ·

8 Douglas Brown,5 and Martin Kolskl

PURPOSE: To describe a radiographic finding-enhancement of the cisternal portion of the third

cranial nerve on postcontrast MR-and to correlate it with patients' clinical symptoms and ultimate

diagnosis. MATERIALS AND METHODS: Thirteen consecutive patients with enhancement of the

cisternal portion of the third cranial nerve on postcontrast MR were retrospectively identified; 50

control patients referred for pituitary microadenomas were also retrospectively reviewed. FIND­

INGS: The enhancement was bilateral in six patients and unilateral in seven patients. Four of the

six patients with bilateral enhancement had unilateral oculomotor nerve palsies; none had bilateral

third cranial nerve palsy. Five of the seven patients with unilateral enhancement had ipsilateral

third nerve palsies. Of the nine patients with third nerve palsies, the pupil was involved in four

patients. Follow-up studies were available in six patients, four of whom had third nerve palsy.

Resolution of the enhancement correlated with resolution of the symptoms in two patients. The

patients ' underlying diagnoses were lymphoma (four), leukemia (one) , viral meningitis (one),

neurofibromatosis (two), inflammatory polyneuropathy-HIV related (one), ophthalmoplegic mi­

graine (one), Tolosa-Hunt syndrome (one), coccidioidomycosis (one), and diabetes (one). No

enhancement was seen in any of the controls. CONCLUSION: Enhancement of the cisternal

segment of the third cranial nerve is always abnormal, revealing an underlying inflammatory or

neoplastic process. However, it is not always associated with clinically apparent oculomotor nerve

dysfunction.

Index terms: Nerves, oculomotor (Ill) ; Contrast media , paramagnetic; Nerves, anatomy; Migraine

AJNR 13:1463-1470, Sep/Oct 1992

The clear depiction of the anatomic course of many of the cranial nerves has become routine on clinical magnetic resonance (MR) imaging. Although lesions of the cranial nerves have been

identified by computed tomography (CT) (1), it is now generally recognized that the diagnostic work-up for suspected cranial nerve pathology

Received June II , 1991; accepted and revisions requested August 9;

revision received December 6. Presented at the 29th Annual Meeting of the ASNR, Washington, DC,

June 9-15, 1991. Department of 1 Radiology, 2 Medicine, and 6 Ophthalmology , Wash­

ington Hospital Center Departments of Radiology, 110 Irving Street, NW,

Washington, DC 2001 0; 3 Hospital of the University of Pennsylvania, 3400

Spruce Street, Philadelphia, PA 19104; 4 Diagnostic Radiology, Stanford

University Hospital , 300 Pasteur Drive, Stanford, CA 94305-5105; and 5 Walter Reed Army Hospital, 6900 Georgia Avenue, NW, Washington,

DC 20307. 7 Current address: Department of Neurology, Georgetown University,

3800 Reservoir Road, Washington, DC 20007. 8 Current address: Wheaton Magnetic Imaging, 2801 University Blvd. ,

Kensington, MD 20815. 9 Address reprint requests to Alexander S. Mark , MD, Department of

Radiology, Washington Hospital Center Department of Radiology , 110

Irving St., NW, Washington, DC 20010.

AJNR 13:1463-1470, Sep/Oct 1992 0195-6108/ 92/ 1305-1463

© American Society of Neuroradiology

must include MR. More recently, contrast en­hancement of the second (2, 3), fifth (4), and seventh (5, 6) cranial nerves on MR has been described in patients with clinically apparent cranioneuropathies. Incidental enhancement of the seventh nerve has also been observed in asymptomatic patients (6) . In this report, we describe gadopentetate dimeglumine diethylen~­triamine pentaacetic acid (Gd-DTP A) enhance-

' ment of the cisternal segment of the third cranial nerve in 13 patients and correlate it with the patients' final diagnoses and clinical findings; 50 normal controls were also studied. The purpose of the paper is to answer two questions: 1) Is the enhancement of the third cranial nerve always abnormal or can it be seen in normal subjects? 2) Is the enhancement of the oculomotor nerve always associated with a clinically apparent third nerve dysfunction?

1463

1464 MARK

Subjects and Methods

Our study included 13 consecutive positive studies (ie, studies that dem onstrated enhancem ent of the cisternal segm ent of the third cranial nerve) collected from four institutions over a period of 3 years.

A 1.5-T system was used for imaging all patients. All patients underwent precontrast axial and/ or coronal T1-weighted images and immediate postcontrast axial and/ or coronal T1 -weighted images (600-800/ 20-25/ 2), 3-mm thick sections with 0- to 1-mm gaps, 256 X 192-256 m atrix, 20- to 22-cm f ield of view. All patients also under­went long TR images (2300/ 30-90/ 1 ), with 5-mm thick sections and 2 .5-mm gap and 256 X 196 m atrix . Gd-DTPA (Berlex Laboratories, Wayne, NJ) 0 .1 mmol/kg was admin­istered intravenously. The m edical records of each patient were reviewed with particular attention to the neurooph­thalmologic exam ination and to the patients' final diagno­sis. Thickening of the third cranial nerve was diagnosed when one of the nerves appeared larger on the precontrast coronal images. No spec ific m easurem ents were used. Enhancem ent of the third cranial nerve was diagnosed when an increase in the intensity of the nerve relative to the precontrast study occurred after contrast administra­tion. In cases of unilateral enhancem ent, the enhancing nerve was brighter than the contralateral one.

For comparison, 50 consecutive adult patients with normal third cranial nerve function referred for suspected pituitary adenomas in one institution (Washington Hospital Center) were evaluated wi th pre- and postcontrast coronal T1 -weighted images using a similar technique. These im­ages were retrospectively evaluated by two neuroradiolo­gists (A.S.M . and D.B.) with particular attention to the m orphology and enhancem ent characteristics of the third cranial nerve.

Results

Our results describing the patients ' age, sex, final diagnosis, presence or absence of bilateral or unilateral third cranial nerve palsy, involve­ment of the pupils, the presence of bilateral or unilateral enhancement, third nerve morphology, other associated symptoms, and associated MR findings , as well as the proof of diagnosis, are listed in Table 1. Of the 13 patients with third cranial nerve enhancement, six patients had bi­lateral enhancement (Figs. 1-3) and seven pa­tients had unilateral enhancement (Figs. 4-8). Four of the six patients with bilateral enhance­ment had unilateral third cranial nerve palsy. None had bilateral third cranial nerve palsy. Five of the seven patients with unilateral enhancement had ipsilateral third cranial nerve palsies. Two patients with unilateral enhancement had neuro­fibromatosis and had normal third cranial nerve function. One patient had a cavernous sinus syn-

AJNR: 13, September / October 1992

drome, including a third cranial nerve palsy. Of the nine patients with third cranial nerve palsies, the pupil was involved in four patients.

Unilateral thickening of the third cranial nerve was noted in four patients on a pre- and post­gadolinium studies. Two patients had neurofibro­matosis and a presumed schwannoma of the third cranial nerve. The other two had an inflammatory process and lymphoma, respectively, involving the third cranial nerve (patients 8 and 1 0). One of the patients with a thickened nerve had bilat­eral enhancement. The patient's symptoms were ipsilateral to the side of oculomotor nerve enlarge­ment.

Follow-up studies were available in six patients (four symptomatic, two asymptomatic), some of whom had interval treatment (see Table 1). In four symptomatic patients, repeat MR studies demonstrated resolution of the enhancement cor­relating with resolution of the symptoms in three patients (who had lymphoma, Tolosa-Hunt, and ophthalmoplegic migraine, respectively); and per­sistence of symptoms in one patient with idi­opathic (? diabetic, ? viral) oculomotor nerve palsy.

In the first asymptomatic patient who had leukemia, repeat MR demonstrated persistent but decreased bilateral enhancement of the oculo­motor nerves following intrathecal chemother­apy. In the other asymptomatic patient who was HIV positive, the enhancement of the oculomotor nerve resolved following zidovudine (AZT, Bur­roughs-Wellcome Co., Research Triangle Park, NC) treatment.

No enhancement of the cisternal segment of the third cranial nerve was encountered on short TR/short TE images in any of the 50 patients referred for evaluation of pituitary microade­noma, all of whom had normal third cranial nerve function. The cisternal segment of the third cra­nial nerve could not be seen on the long TR images in the normal and abnormal patients be­cause of their thickness (5 mm) and interstice gap (2.5 mm).

Discussion

The imaging of cranial neuropathies has been dramatically improved with the refinement of high resolution MR. Although morphologic alter­ations of the cranial nerves can sometimes be seen, many reports suggest that intravenous con­trast plays an important role in the diagnosis of cranial nerve pathology (2-6). Enhancement of

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1466 MARK AJNR: 13, September / October 1992

A B c Fig. 1. Patient 2; 67-year-old woman with chronic lymphocytic leukemia; no third cranial nerve palsy . Axial pre- (A) and post­

gadolinium (B) Tl -weighted (600/ 20) images demonstrate bilateral enhancement of the third nerves (arrows). Axial Tl-weighted image (C) postintrathecal chemotherapy shows decreased but persistent enhancement (curved arrows).

Fig. 2. Case 4; 34-year-old man-HIV positive and lymphoma proven by bone marrow biopsy . Right third nerve palsy . Pre­(A) and postcontrast (B) contrast Tl­weighted (600/ 20) axial images demonstrate enhancement of the third cranial nerves.

Fig. 3. Case 6; 49-year-old HIV positive man with an inflammatory polyneuropathy resulting in diffuse arm and leg weakness and a right facial weakness. No diplopia. Pre­( A) and postcontrast (B) Tl -weighted (600/ 20) axial MR demonstrates enhancement of the third cranial nerves. Enhancement of the right seventh cranial nerve in the temporal bone was also demonstrated on the lower sections.

the second, fifth , and seventh cranial nerves on contrast-enhanced MR has been reported in pa­tients with neuropathies of these nerves second­ary to a variety of inflammatory or neoplastic processes (2-6). The enhancement has been as­sociated with viral neuropathies, in particular her­pes (4), Bell 's palsy (5 , 6), syphilis (7), as well as demyelinating optic neuritis and post-radiation

optic neuritis (2 , 3). However, we, as well as other authors (6), have occasionally encountered en­hancement of the seventh cranial nerve in asymp­tomatic patients with no apparent underlying pa­thology.

Since we have not observed enhancement of the third cranial nerve in any of our controls and since all 13 patients had an underlying disease

AJNR: 13, September / October 1992

Fig. 4. Patient 3; 74-year-old woman with left parenchymal lymphoma (black arrow) and a right third cranial nerve palsy . Coronal post-gadolinium Tl -weighted (600/ 20) images. Notice enhancement of the right oculomotor nerve (white arro w).

and/ or a third cranial nerve palsy, our study suggests that enhancement of the third cranial nerve is always abnormal, indicating an underly­ing inflammatory or neoplastic pathology.

Enhancement of the oculomotor nerve, how­ever, is not always associated with a clinically apparent third nerve palsy. Furthermore, while resolution of the enhancement was associated with resolution of the third cranial nerve palsy in some patients, in two patients the symptoms persisted and/ or recurred while the enhancement resolved (patients 10 and 11). Four of the nine patients with third cranial nerve palsy had in­volvement of the pupil , whereas the other five had normal pupillary function. The parasympa­thetic fibers travel on the superficial aspect of the oculomotor nerve in the cisternal portion and are most susceptible to extrinsic compression by extraneural masses such as posterior communi­cating artery aneurysms. Conversely, in 68 % to 86% of cases due to infarction of the microvas­culature located centrally in the nerve, the pupil­lary fibers are spared (8). These clinical findings are not absolute. In 3% to 5 % of aneurysms, the pupil may be spared (8).

In our series, only one patient was diabetic (patient 11). The persistence of the palsy 1 year after the initial presentation is unusual since most such patients recover after several months (8). Persistence of the palsy beyond this time sug­gests a different cause for the third cranial nerve palsy. The low incidence of diabetic microvas-

OCULOMOTOR NERVE ENHANCEMENT ON MR 1467

cular infarcts in our series may be explained by the fact that most diabetic patients with pupil­sparing third cranial nerve palsies do not undergo MR. However, we have studied three diabetic patients with acute pupil-sparing third cranial nerve palsies using a similar MR technique and did not observe any enhancement of the third cranial nerve. Thus, it is unlikely the palsy in patient 11 is diabetic in origin. Additional studies are necessary to determine the incidence of oc­ulomotor nerve enhancement in diabetic micro­vascular infarct third cranial nerve palsies.

Third cranial nerve palsy in patients with AIDS has been previously reported (9 , 10). The palsy may be due to an intraaxial mass lesion such as parenchymal toxoplasmosis or lymphoma affect­ing the midbrain in the region of the third cranial nerve nucleus, or as demonstrated by patient 6, direct involvement of the third cranial nerve by HIV as suggested by the resolution of the en­hancement on the post-AZT study. In patients with CNS lymphoma, the enhancement of the third cranial nerve probably reflects coating and/ or infiltration of the nerve by lymphomatous cells.

The two patients with neurofibromatosis and presumed third cranial nerve schwannomas were both asymptomatic with respect to oculomotor nerve function . They both had many other schwannomas diagnosed by gadolinium-en­hanced MR. The diagnosis is often clinically ob­vious and enhancement of the third cranial nerve may be only one of many findings . In such cases, the depiction of a third cranial nerve-enhancing lesion would be without a great deal of clinical significance. However, isolated oculomotor nerve schwannomas may be symptomatic, presenting with third cranial nerve palsy ( 11 ).

In the past, a number of nondiabetic and non­myasthenic patients with third cranial nerve pal­sies and negative arteriograms and CT scans were categorized as idiopathic , and an inflammatory or "vascular" process was suspected. These condi­tions are nevertheless important since the pupil is often involved, suggesting a compressive lesion (8). Our study suggests that such inflammatory processes may now be imaged by gadolinium­enhanced MR.

Ophthalmoplegic migraine is a rare cause of third cranial nerve palsy (12). Miller, in a review of 3 million admissions at Johns Hopkins Hospi­tal , found 30 cases of isolated third cranial nerve palsy in children, two of which were diagnosed as ophthalmoplegic migraines (13). It is a diag­nosis of exclusion, traditionally requiring a typical

1468 MARK AJNR: 13, September/October 1992

A 8 c

Fig. 5. Patient 7; 7-year-old girl with severe headache, nausea, vomiting, and a right third cranial nerve palsy. Clinical diagnosis: ophthalmoplegic migraine. Precontrast parasaggital (A) T1-weighted image through the right third nerve (curved arrow). Postcontrast coronal (B), parasagittal (C), and axial (D) T1-weighted (600/20) images demonstrate enhancement of the third cranial nerve (arrows) and of the pia in the interpeduncular cistern. Follow-up coronal (E) 3 weeks later demonstrates resolution of the enhancement of the anterior aspect of the third cranial nerve (curved arrow); minimal residual enhancement of the posterior aspect of the nerve and pia in the interpeduncular ·cistern is still present (curved arrow) on the para sagittal image (F). A phase encoding artifact is seen just below the third cranial nerve (straight arrow). The patient's symptoms resolved spontaneously. ·

8

Fig. 6. Case 8; 24-year-old woman with unilateral headache and third cranial nerve palsy. Coronal (A) and parasagittal (B) contrast­enhanced T1-weighted (600/ 20) images demonstrate enhancement of the right third cranial nerve (arrows). Follow-up study, coronal (C) 1 month later after steroid treatment demonstrates resolution of the third cranial nerve enhancement. The symptoms resolved. Clinical diagnosis: Tolosa-Hunt syndrome.

AJNR: 13, September / October 1992 OCULOMOTOR NERVE ENHANCEMENT ON MR 1469

Fig. 7. Case 12; 56-year-old man with right-sided third nerve palsy involving the pupil. Arteriography was negative. Axial Tl­weighted image (600/20) demonstrates enhancement of the cis­ternal segment of the right third cranial nerve (white curved arrow). Notice the enhancement along the pia of the right temporal lobe (black curved arrow), and interpeduncular cistern (straight black arrow). Cerebrospinal fluid studies confirm the diagnosis of coccidioidomycosis.

Fig. 8. Case 9; 35-year-old man with neurofibromatosis and oculomotor nerve palsy . Axial short TR/ TE (600/ 20) MR shows enhancing right third nerve mass (blqck arrows) arising from interpeduncular cistern in patient with neurofibromatosis. Also note enhancing right fourth nerve mass (white arrows) coursing around midbrain from dorsal aspect of perimesencephalic cistern .

history of migraine and a normal arteriogram to exclude an aneurysm. Atypical forms without the accompanying headaches have been described as a variant of ophthalmoplegic migraine (14). The etiology of this condition remains obscure. Certain authors suggested that narrowing of the carotid artery in the cavernous sinus produced edema that may compress the third cranial nerve (15). Other authors believe it is due to delayed ischemic neuropathy (16). The location of the enhancement in patient 6 at the origin of the third cranial nerve in the interpeduncular cistern is clearly not consistent with this hypothesis. Additional studies will be necessary to elucidate the nature of this clinical syndrome.

T olosa-Hunt syndrome is a clinical condition characterized by retro-orbital pain and variable

degrees of ophthalmoplegia with or without de­crease in vision ( 17). Although the characteristic clinical presentation in these patients is a cavern­ous sinus or an orbital apex syndrome, an isolated third cranial nerve palsy (as in patient 8) can occasionally be seen. Until the advent of high­resolution of MR, Tolosa-Hunt syndrome was also often a diagnosis of exclusion after arteriography confirmed the absence of an aneurysm. Recently , the MR appearance of Tolosa-Hunt syndrome has been reported ( 17). Enhancement and abnormal soft tissue in the ipsilateral cavernous sinus is usually noted. This appearance is nonspecific since lymphoma, sarcoidosis, and other neoplas­tic conditions can have a similar radiographic appearance. In these patients, the cavernous sinus usually returns to normal radiographically either spontaneously or after steroid treatment. Enhancement of the cisternal segment of the oculomotor nerve in T olosa-Hunt syndrome has not been previously reported and the significance of this finding is unclear. One can speculate that there may be some overlap clinically between T olosa Hunt syndrome and ophthalmoplegic mi­graine, especially the "variant" form.

Viral meningitis, as in patient 1, may also produce a third cranial nerve palsy. By demon­strating meningeal enhancement, MR suggested the correct diagnosis, differentiating this condi­tion from other inflammatory processes affecting the oculomotor nerve primarily.

From our observations, it is apparent that the role of MR in the evaluation of patients with third nerve palsies is rapidly evolving. As with any other cranial neuropathy, when imaging these patients it is important to evaluate the entire course of the nerve from its nucleus through the cisternal portion, cavernous sinus, and to the orbital apex. MR is uniquely suited for this task (18). The most serious potential cause for a third nerve palsy is an aneurysm originating from the origin of the posterior communicating artery. At the present time, the sensitivity of MR angiogra­phy for the detection of these aneurysms is not known. Because of the potentially devastating consequence of missing such an aneurysm, we believe that in a patient with a third cranial nerve palsy involving the pupil, arteriography is the initial modality of choice to exclude an aneurysm. This approach may change if MR angiography proves itself a reliable diagnostic tool for aneu­rysm detection. If an aneurysm is excluded in a patient with pupillary involving oculomotor palsy, MR with contrast should be the next imaging

1470 MARK

study. Likewise, in patients with pupillary-sparing third cranial nerve palsy who are neither diabetic nor myasthenic, MR with contrast may be ex­tremely useful in detecting neoplastic or inflam­matory processes in the oculomotor nerve and direct further investigation.

Acknowledgments

We would like to thank Lori Baker, MD, Robert Tash, MD, and Charles Fitz, MD, for providing a case each, and Nancy Carnes for editorial assistance.

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